论文部分内容阅读
近年来发现,IFN-Y可与IL-2/INF-a/TNF-B/LP协同诱导巨噬细胞(M)产生大量的一氧化氦(NO)。NO作为活化M的一种细胞毒效应分子,在抑制和杀伤寄生虫的杭感染免疫中起重要作用。NO通过作用于宿主细胞的线粒体呼吸酶、DNA合成酶及顺乌头酸酶,与这些酶的活性部位一Fe-S基结合,形成铁-亚硝酰基复合物,抑制酶的活性,从而阻断靶细胞的能量合成及DNA复制,引起宿主细胞的死亡。
It has been found in recent years that IFN-γ synergizes with IL-2 / INF-a / TNF-B / LP to induce macrophage (M) to produce large amounts of nitric oxide (NO). NO, a cytotoxic effector molecule that activates M, plays an important role in the suppression and killing of parasitic Hang-infected immunity. NO acts on the host cell mitochondrial respiratory enzyme, DNA synthase and aconitase, with the active site of these enzymes a Fe-S group to form iron - nitrosyl complexes, inhibit the activity of the enzyme, which resistance Disruption of target cell energy synthesis and DNA replication, leading to the death of host cells.